There is strong evidence that the destruction of syngeneic tumors may be mediated by at least 3 distinct effector mechanisms which involve T cells, null cells, and macrophages as the effectors. There is also evidence that each of these effector mechanisms can be and are suppressed in tumor bearing hosts by suppressive factors released by the tumors or by suppressor cells induced by direct contact with tumors or by "blocking factors" present in the serum of the tumor bearing host. The first objective of this project is to examine the interactions of phenotypically distinct subpopulations of cells which are involved in the generation and suppression of three different immune mechanisms effecting the destruction of syngeneic tumors. The second objective is to determine how a syngeneic tumor subverts those interactions or interferes with those mechanisms so as to escape destruction. Th basic approach to these objectives is to examine the changes in functional activity, induced by in vivo or in vitro exposure to syngeneic tumors, of lymphocytes and monocyte subpopulations isolated by cell sorting on the basis of the presence or absence of surface Fc, complement, and cytophilic antibody receptors. Since the cells bearing these receptors have been implicated in effector or suppressor mechanisms of tumor immunity, these studies will elucidate the interactions of these cells required for generation of anti-tumor effectors and the role of the receptors both in those interactions as well as in the mechanisms by which syngeneic tumors subvert or disrupt those interactions.